Relatively little is known about the neurobiology of insomnia, despite its wide prevalence and broad medical impact. Although much is still to be learned about the pathophysiology of the disorder, identification, systematic assessment, and appropriate treatment are clearly beneficial to patients. Recent research, using quantitative EEG, polysomnography (PSG), multiple sleep latency test (MSLT) and neuroimaging techniques, suggests that some broad areas can be identified as possible pathophysiological models. Sleep-wake homeostat model hypothesizes a failure in homeostatic regulation of sleep, an attenuated increase in sleep drive with time awake, and/or defective sensing of sleep need. Circadian clock model hypothesizes a dysfunctional circadian clock, resulting in changes in the timing of sleep-wake propensity that are incompatible with normal sleep. Intrinsic sleep-wake state mechanism model suggests that abnormal function of insomnia comprises the systems responsible for expression of the sleep states themselves. Extrinsic over-ride mechanism (stress-response) model suggests that insomnia reflects the consequences of overactivity of one of the systems considered "extrinsic" to normal sleep-wake control. Many current therapies for insomnia are based on these physiological models. Several attempts have been made to create a physiological model that would explain this disorder and could be used as a foundation for treatment. However, it appeared that no model can fully explain and clarify all aspects of insomnia. Future research should be necessary to expand our knowledge on the biological dimensions of insomnia.
Circadian Clocks ; Electroencephalography ; Humans ; Neurobiology ; Neuroimaging ; Polysomnography ; Prevalence ; Sleep Initiation and Maintenance Disorders

No abstract available.
Organization and Administration* ; Psychotherapy*

No abstract available.
Movement Disorders* ; Prevalence*

No abstract available.
Organization and Administration* ; Psychotherapy*

The most common pathogen of respiratory tract infection among school-age children and adolescents is Mycoplasma pneumoniae, which causes clinical manifestations of pneumonia, acute asthmatic attack, pharygitis, and tonsilitis. It can also cause extrapulmonary infections that involves skin, the nervous system, the digestive system, the cardiovascular system, and the hematopoietic system. It is reported that the central nervous system symptoms may occur in 0.1% to 7% of patients hospitalized with Mycoplasma pneumoniae infection. Direct invasion, toxin, immune-mediated, and vascular phenomenon have been proposed for the etiology of the neurological manifestations. We have experienced a six-year-old male patient with Mycoplasma pneumoniae pneumonia who had complained of both leg pains and immobility two weeks after the onset of pneumonia, which was confirmed as peripheral neuropathy of Guillain-Barr syndrome. Three weeks after the disease-onset, altered consciousness and seizure attacks developed and intravenous immunoglobulins infused under the impression of encephalitis induced by Mycoplasma pneumoniae infection. He showed complete recovery of running and mentality five months after the disease-onset. We herein report a case of Mycoplasma pneumoniae pneumonia complicated with Guillain-Barr Syndrome and encephalitis about 2 or 3 weeks after the disease onset with a review of literatures.
Adolescent ; Cardiovascular System ; Central Nervous System ; Child ; Consciousness ; Digestive System ; Encephalitis* ; Guillain-Barre Syndrome* ; Hematopoietic System ; Humans ; Immunoglobulins ; Immunoglobulins, Intravenous ; Leg ; Male ; Mycoplasma pneumoniae* ; Mycoplasma* ; Nervous System ; Neurologic Manifestations ; Palatine Tonsil ; Peripheral Nervous System Diseases ; Pneumonia* ; Pneumonia, Mycoplasma* ; Respiratory Tract Infections ; Running ; Seizures ; Skin

OBJECTIVE: Panic disorder has been suggested to be divided into the respiratory and non-respiratory subtypes in terms of its clinical presentations. The present study aimed to investigate whether there are any differences in treatment response and clinical characteristics between the respiratory and non-respiratory subtypes of panic disorder patients. METHODS: Among the 48 patients those who completed the study, 25 panic disorder patients were classified as the respiratory subtype, whereas 23 panic disorder patients were classified as the non-respiratory subtype. All patients were treated with escitalopram or paroxetine for 12 weeks. We measured clinical and psychological characteristics before and after pharmacotherapy using the Panic Disorder Severity Scale (PDSS), Albany Panic and Phobic Questionnaire (APPQ), Anxiety Sensitivity Index-Revised (ASI-R), State-Trait Anxiety Inventory (STAI-T, STAI-S), Hamilton Anxiety Rating Scale (HAM-A), and Hamilton Depression Rating Scale (HAM-D). RESULTS: The prevalence of the agoraphobia was significantly higher in the respiratory group than the non-respiratory group although there were no differences in gender and medication between the two groups. The respiratory group showed higher scores on the fear of respiratory symptoms of the ASI-R. In addition, after pharmacotherapy, the respiratory group showed more improvement in panic symptoms than the non-respiratory group. CONCLUSION: Panic disorder patients with the respiratory subtype showed more severe clinical presentations, but a greater treatment response to SSRIs than those with non-respiratory subtype. Thus, classification of panic disorder patients as respiratory and non-respiratory subtypes may be useful to predict clinical course and treatment response to SSRIs.
Agoraphobia ; Anxiety ; Citalopram ; Classification ; Depression ; Drug Therapy ; Humans ; Panic ; Panic Disorder* ; Paroxetine ; Prevalence ; Surveys and Questionnaires ; Serotonin Uptake Inhibitors ; Treatment Outcome

OBJECTIVE: This study was aimed to compare the efficacy and tolerability of milnacipran and sertraline treatment in patients with major depressive disorder and to evaluate the relationships between beta-adrenergic receptor responsiveness and depressive mood states. METHODS: Fifty three patients who had a diagnosis of major depressive disorder according to the DSM-IV and showed scores of 17 or more on the 17-item Hamilton Rating Scale for Depression (HAM-D) were randomly assigned to either milnacipran or sertraline treatment group. Each patient received 8 weeks of antidepressant treatment with one of the two drugs. Efficacy was assessed using the HAM-D, Beck Depression Inventory (BDI), Montgomery and Asberg Depression Rating Scale (MADRS) and Clinical Global Impression (CGI). Twenty normal control subjects who had no history of psychiatric and major medical illness and were matched with the depressed patients considering age, sex and body mass index were recruited for the comparison of beta-adrenergic receptor responsiveness between depressed patients and normal control subjects. We measured beta-adrenergic receptor density, lymphocyte cAMP ratio (ratio of isoproterenol-stimulated cAMP/basal cAMP), and receptor affinity (Kd) in all subjects. We also investigated beta-adrenergic receptor responsiveness before and after treatment in depressed patients. RESULTS: Twelve patients in milnacipran group and 15 patients in sertraline group were completed this study. In all assessment scales for depression, we found significant decrease in depression severity in both milnacipran and sertraline groups. Both of the two drugs proved equally effective for reduction of the overall symptoms of depression throughout the treatment period. And there were significant differences in the means of Kd values between control subjects and depressed patients before treatment. We found a significant negative correlation between Kd values and BDI scores. After treatment with either milnacipran or sertraline, cAMP ratio (4.8+/-1.6 vs 5.7+/-2.5, p=0.095) and Kd value (65.6+/-11.9 vs 74.6+/-7.8, p=0.066) tended to increase, but there was no significant difference in beta-adrenergic receptor responsiveness between milnacipran and sertraline group. CONCLUSION: Both milnacipran and sertraline were not different in the clinical efficacy in major depressive disorder. In depressed patients, beta-adrenergic receptor responsiveness is reduced and both milnacipran and sertraline antidepressants tended to increase beta-adrenergic receptor responsiveness.
Antidepressive Agents ; Body Mass Index ; Depression ; Depressive Disorder, Major* ; Diagnosis ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Lymphocytes ; Sertraline* ; Weights and Measures

OBJECTIVE: There have been many studies to show the close relationship between anxiety and beta-adrenergic receptor function in patients with anxiety disorder. This study examined the relationship between anxiety levels and beta-adrenergic receptor function in a normal population. METHODS: Subjects for this study were 18 men and 28 women from 20 to 40 years of age whose body mass index was between 17.525 and 26.145. All of them were healthy subjects who had no previous history of medical or psychiatric illnesses. We measured the Korean versions of Spielberger State-Trait Anxiety Inventory and Beck Depression Inventory, and a self-report form of physical fitness level. We also measured the Chronotrophic 25 Dose (CD 25) of isoproterenol, previously developed to assess in vivo beta-adrenergic receptor sensitivity. RESULTS: The mean of CD 25 was 2.5 (+/-1.2)microgram, and there was a significant difference in the mean of CD 25 between men and women (t (17)= -3.73, p=0.0009). This gender difference in beta-adrenergic receptor sensitivity might be accounted for by different means of body mass index between men and women. The correlations between CD 25 and state anxiety levels (r=-0.3966, p=0.0064) and between CD 25 and trait anxiety levels (r=-0.3918, p=0.0071) were both statistically significant. The CD 25 was also positively correlated with age (r=0.4827, p=0.0007) and body mass index (r=0.3517, p=0.0166). CONCLUSION: The sensitivity of beta-adrenergic receptors increased as anxiety levels became higher in a normal population. Thus, the relationship between anxiety and beta-adrenergic function in healthy subjects seemed to be different from that in patients with anxiety disorder. This result suggests that we need a new hypothetical model in order to explain how anxiety affects beta-adrenergic receptors in both healthy subjects and patients with anxiety disorder.
Anxiety Disorders ; Anxiety* ; Body Mass Index ; Depression ; Female ; Humans ; Isoproterenol ; Male ; Physical Fitness ; Receptors, Adrenergic* ; Receptors, Adrenergic, beta

Although serotonin reuptake inhibitors (SRIs) are the primary therapeutic drugs for obsessive compulsive disorder (OCD), as many as 40% (up to 60%) of OCD patients do not show an adequate response to these drugs. SRI-refractory patients with OCD may have abnormalities in their central dopaminergic system as well as serotonergic system. The combination therapy with SRIs and antipsychotic drugs is considered to be effective especially for treatment-refractory OCD patients who have comorbid tic disorders or schizotypal personality disorder. Recently, the augmentation of atypical antipsychotics has been suggested to be effective in treating SRI-refractory OCD patients, and risperidone and olanzapine could be promising drugs for SRI-refractory OCD patients. We reviewed recent literatures regarding the clinical efficacy of atypical antipsychotics for treatment-refractory OCD patients.
Antipsychotic Agents* ; Humans ; Obsessive-Compulsive Disorder* ; Risperidone ; Schizotypal Personality Disorder ; Serotonin Uptake Inhibitors ; Tic Disorders

OBJECTIVES: Previons studies reported altered beta-adrenergic receptor (betaAR) responsiveness in panic disorder, but few studies reported to see the effect of pharmacotherapy on betaAR function in panic patients. This investigation examined betaAR responsiveness in patients with panic disorder before and after pharmacotherapy with paroxetine. METHODS: After assessment using the Anxiety Disorder Interview Schedule for DSM-IV, 27 acute panic patients whose illness duration did not exceed 1 year were assigned to 12 weeks of paroxetine treatment. Twenty seven normal control subjects with no previous history of major medical and psychiatric illnesses were matched by age, sex, exercise, and body mass index. The Hamilton rating scale for anxiety (HAM-A), Hamilton rating scale for depression (HAM-D), Spielberger state-trait anxiety inventory-State (STAI-S) and Trait (STAI-T), acute panic inventory (API), anxiety sensitivity index (ASI), and Beck depression index (BDI) were performed to assess clinical states in the panic patients before and after treatment. The HAM-A, HAM-D, STAI-S and STAI-T, and BDI were also performed in the normal control subjects. We measured the betaAR density (Bmax), affinity (1/Kd), and sensitivity (cyclic AMP ratio of isoproterenol-stimulated cAMP to basal cAMP) in all subjects. RESULTS: Panic patients showed much lower scores of the HAM-A, STAI-S, STAI-T, API, ASI, HAM-D, and BDI after 12 weeks of paroxetine treatment than those before the treatment. There was no significant difference in the means of Bmax and cAMP ratio between control subjects and panic patients before and after the treatment. However, pretreatment Kd (R2=0.314, beta=-0.876, p=0.001) and Bmax (R2=0.230, beta=-0.575, p=0.019) significantly accounted for API scores after the treatment and change of Bmax according to the treatment accounted for the improvement of anxiety sensitivity (R2=0.353, beta=0.594, p=0.015). The pretreatment Kd value was significantly higher in the panic patients compared with that of control subjects (78.35+/-26.20 vs. 59.15+/-29.33, p=0.014), which was significantly reduced after the treatment (79.43+/-26.83 vs. 56.38+/-28.79, p=0.002). The pretreatment Kd value significantly accounted for the improvement of API scores (R2=0.316, beta=0.562, p=0.029) and the decrease in trait anxiety (R2=0.246, beta=-0.513, p=0.025). CONCLUSION: In acute panic patients, only betaAR affinity was reduced before the treatment, which was contrary to our expectation. Decreased betaAR affinity was normalized after paroxetine treatment. Decreased betaAR affinity and increased betaAR density before the treatment predicted good treatment response in acute panic patients. Thus, betaAR affinity and density could be useful biological markers that predict the treatment response of paroxetine in panic disorder.
Anxiety ; Anxiety Disorders ; Appointments and Schedules ; Biomarkers* ; Body Mass Index ; Depression ; Diagnostic and Statistical Manual of Mental Disorders ; Drug Therapy ; Humans ; Panic Disorder* ; Panic* ; Paroxetine* ; Receptors, Adrenergic, beta